Androgens and cardiac diseases

Although androgens have been considered deleterious for the cardiovascular system, recent data have demonstrated favourable testosterone effects on cardiac and vascular remodeling and clinical outcome. However, the cardiovascular risk-benefit profile of testosterone therapy remains largely elusive due to lack of well-designed and adequately powered randomized clinical trials. In any case, a large body of clinical evidence underlines that low plasma testosterone levels should be considered a risk factor for cardiovascular disease, and that the evaluation of sex steroids should be included in the routine clinical evaluation of cardiac patients. A better understanding of the mechanism regulating the effects of testosterone on cardiovascular system could lead to novel therapeutic strategies in several cardiac patient populations, such as chronic heart failure patients and those who recently underwent cardiac surgery

A multicenter, randomized, controlled trial on short-term feasibility and impact on functional capacity, symptoms and neurohumoral activation

RE-START is a multicenter, randomized, prospective, open, controlled trial aiming to evaluate the feasibility and the short- and medium-term effects of an earlystart AET program on functional capacity, symptoms and neurohormonal activation in chronic heart failure (CHF) patients with recent acute hemodynamic decompensation. Study endpoints will be: 1) safety of and compliance to AET; 2) effects of AET on i) functional capacity, ii) patient- reported symptoms and iii) AET-induced changes in beta-adrenergic receptor signaling and circulating angiogenetic and inflammatory markers. Two-hundred patients, randomized 1:1 to training (TR) or control (C), will be enrolled. Inclusion criteria: 1) history of systolic CHF for at least 6 months, with ongoing acute decompensation with need of intravenous diuretic and/or vasodilator therapy; 2) proBNP >1000 pg/ml at admission. Exclusion criteria: 1) ongoing cardiogenic shock; 2) need of intravenous inotropic therapy; 3) creatinine >2.5 mg/dl at admission. After a 72-hour run-in period, TR will undergo the following 12-day early-start AET protocol: days 1-2: active/passive mobilization (2 sessions/day, each 30 minutes duration); days 3-4: as days 1-2 + unloaded bedside cycle ergometer (3 sessions/day, each 5-10 minutes duration); days 5-8: as days 1-2 + unloaded bedside cycle ergometer (3 sessions/day, each 15-20 minutes duration); days 9-12: as days 1-2 + bedside cycle ergometer at 10-20 W (3 sessions/day, each 15-20 minutes duration). During the same period, C will undergo the same activity protocol as in days 1-2 for TR. All patients will undergo a 6- minWT at day 1, 6, 12 and 30 and echocardiogram, patient- reported symptoms on 7-point Likert scale and measurement of lymphocyte G protein coupled receptor kinase, VEGF, angiopoietin, TNF alfa, IL-1, IL-6 and eNOS levels at day 1, 12 and 30

Baseline and exercise predictors of VO2peak in systolic heart failure patients : Results from SMARTEX-HF

Author's accepted version (postprint).This is an Accepted Manuscript of an article published by American College of Sports Medicine in Medicine & Science in Sports & Exercise on 04/11/2019.Available online: https://journals.lww.com/acsm-msse/FullText/2020/04000/Baseline_and_Exercise_Predictors_of_V_O2peak_in.5.aspxacceptedVersio

Recomendações Europeias para a prevenção da doença cardiovascular na prática clínica (versão de 2012)

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Sex Profile and Risk Assessment With Cardiopulmonary Exercise Testing in Heart Failure: Propensity Score Matching for Sex Selection Bias

In heart failure (HF), women show better survival despite a comparatively low peak oxygen consumption (V ̇o2): this raises doubt about the accuracy of risk assessment by cardiopulmonary exercise testing (CPET) in women. Accordingly, we aimed to check (1) whether the predictive role of well-known CPET risk indexes, ie, peak V ̇o2 and ventilatory response (V ̇e/V ̇co2 slope), is sex independent and (2) if sex-related characteristics that impact outcome in HF should be considered as associations that may confound the effect of sex on survival

Cardiac rehabilitation and exercise training

Secondary prevention programmes are delivered as cardiac rehabilitation or other prevention programmes for all patients with cardiovascular disease or at high risk for cardiovascular disease. Cardiac rehabilitation is defined as a comprehensive programme involving exercise training, risk factor modification, education, and psychological support. The core components and goals of cardiac rehabilitation have been standardized, but the structure, length, and type of programme offered differs widely by country, affected by national guidelines and standards, legislation, and payment factors.</p

Different Determinants of Ventilatory Inefficiency at Different Stages of Reduced Ejection Fraction Chronic Heart Failure Natural History

Background It is not known whether determinants of ventilation ( VE )/volume of exhaled carbon dioxide ( VCO 2 ) slope during incremental exercise may differ at different stages of reduced ejection fraction chronic heart failure natural history. Methods and Results VE / VCO 2 slope was fitted up to lowest VE / VCO 2 ratio, that is, a proxy of the VE /perfusion ratio devoid of nonmetabolic stimuli to ventilatory drive. VE / VCO 2 slope tertiles were generated from our database (&lt;27.5 [tertile 1], ≥27.5 to &lt;32.0 [tertile 2], and ≥32.0 [tertile 3]), and 147 chronic heart failure patients with repeated tests yielding VE / VCO 2 slopes in 2 different tertiles were selected. Determinants of VE / VCO 2 slope changes across tertile pairs 1 versus 2, 2 versus 3, and 1 versus 3 were assessed by exploring changes in VE and VCO 2 at lowest VE / VCO 2 and those in VE /work rate (W) and VCO 2 /W slope. Resting and peak cardiac output ( CO ) were calculated as VO 2 /estimated arteriovenous O 2 difference and the CO /W slope analyzed. Notwithstanding a progressively lower W with increasing tertile, VE at lowest VE / VCO 2 and VE /W slope were significantly higher in tertiles 2 and 3 versus tertile 1. Conversely, VCO 2 at lowest VE / VCO 2 and CO /W slope significantly decreased across tertiles, whereas VCO 2 /W slope did not. Difference (Δ) in VE /W slope between tertiles accounted for 71% of Δ VE / VCO 2 slope variance, with Δ VCO 2 /W slope explaining an additional 26% (model r =0.99; r 2 =0.97; P &lt;0.0001). Similar results were obtained substituting Δ VCO 2 /W slope with Δ CO /W slope. Conclusions Ventilatory overactivation is the predominant cause of VE / VCO 2 slope increase at initial stages of chronic heart failure, whereas hemodynamic impairment plays an additional role at more‐advanced pathophysiological stages. </jats:sec